This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kerr, A. R. Articles by Mitchell, T. J. Search for Related Content PubMed PubMed Citation Articles by Kerr, A. R. Articles by Mitchell, T. J.

 Previous Article  |  Next Article 

Infection and Immunity, July 2005, p. 4245-4252, Vol. 73, No. 7
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.7.4245-4252.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Innate Immune Defense against Pneumococcal Pneumonia Requires Pulmonary Complement Component C3

Division of Infection and Immunity, IBLS, University of Glasgow, Glasgow G12 8QQ, United Kingdom

Received 6 December 2004/ Returned for modification 14 January 2005/ Accepted 21 February 2005

Complement is known to be involved in protection against systemic infection with Streptococcus pneumoniae. However, less is known about effects of complement within the lungs during pneumococcal pneumonia. By intranasally infecting transgenic mice unable to express complement C3, we investigated the role of complement in pulmonary defenses against S. pneumoniae. It was demonstrated that within the lungs, there is a requirement for C3 during the initial hours of infection. It was found that within 1 h of infection, bacterial loads decreased within lung airways of control mice as C3 protein increased. The lack of C3 resulted in the inability to control growth of wild-type or attenuated pneumococci within the lungs and bloodstream, resulting in an overwhelming inflammatory response and shorter survival times. Our results show that during the initial hours of infection with S. pneumoniae, C3 is protective within the lungs and subsequently plays an important role systemically.

Editor: J. N. Weiser

This article has been cited by other articles:

• Jiang, Z., Huang, W., Li, J., Li, M., Liang, A., Zhang, S., Chen, B. (2008). Nanogold Catalysis Based Immunoresonance-Scattering Spectral Assay for Trace Complement Component 3. Clin. Chem. 54: 116-123 [Abstract] [Full Text]  
• Pasupuleti, M., Walse, B., Nordahl, E. A., Morgelin, M., Malmsten, M., Schmidtchen, A. (2007). Preservation of Antimicrobial Properties of Complement Peptide C3a, from Invertebrates to Humans. J. Biol. Chem. 282: 2520-2528 [Abstract] [Full Text]  
• Kerr, A. R., Paterson, G. K., McCluskey, J., Iannelli, F., Oggioni, M. R., Pozzi, G., Mitchell, T. J. (2006). The Contribution of PspC to Pneumococcal Virulence Varies between Strains and Is Accomplished by Both Complement Evasion and Complement-Independent Mechanisms. Infect. Immun. 74: 5319-5324 [Abstract] [Full Text]